Ginsenoside compound K ameliorates imiquimod-induced psoriasis like dermatitis through inhibiting REG3A/RegIIIγ expression in keratinocytes
Ginsenoside compound K ameliorates imiquimod-induced psoriasis like dermatitis through inhibiting REG3A/RegIIIγ expression in keratinocytes
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人参皂苷化合物 K 通过抑制角质形成细胞中 REG3A/RegIII gamma 表达来改善咪喹莫特诱导的银屑病样皮炎
DOI：
10.1016/j.bbrc.2019.06.007
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发表时间：
2019-08-06
影响因子：
3.1
通讯作者：
Shi, Yuling
中科院分区：
文献类型：
--
作者：
Fan, Huayu;Wang, Yao;Shi, Yuling
背景：银屑病是一种以角质细胞过度增生为特征的慢性炎症性皮肤病。人参皂苷化合物K （CK）是人参的一种生物活性代谢物，通过影响角质细胞生物学来调节各种皮肤疾病。然而，人参皂苷CK对银屑病的治疗作用尚未见研究。目的：我们的目的是研究人参皂苷CK是否会影响角质形成细胞的稳态和银屑病相关抗菌蛋白再生胰岛衍生蛋白3- α (REG3A)及其同源物regii γ的表达。我们进一步探讨了人参皂苷CK在咪喹莫特（IMQ）诱导的银屑病样皮炎中的治疗潜力。方法：采用MTT法和流式细胞术分别检测人参皂苷CK对人角质形成细胞生长和凋亡的影响。Western blot检测人参皂苷CK刺激后HaCaT细胞Bax水平。白细胞介素(IL)-36 γ和人参皂苷CK联合模拟后，采用RT-PCR和Western blot方法评估人角质形成细胞中REG3A的水平。利用imq诱导的银屑病小鼠模型，通过皮肤厚度和组织学检查评估0.1%和1%人参皂苷CK乳膏的治疗效果，并采用Western blot和免疫荧光法检测病变皮肤中的RegIII γ水平。结果：人参皂苷CK抑制人角质细胞增殖，但不影响细胞凋亡。此外，它还能抑制1L-36 γ诱导的HaCaT细胞中REG3A的表达。人参皂苷CK减轻吡喹莫德诱导的银屑病样角化过度，并降低病变皮肤角化细胞中RegIII γ的表达。结论：人参皂苷CK可能通过抑制角化细胞中REG3A/RegIII γ的表达来改善imq诱导的银屑病样皮炎，提示人参皂苷CK在银屑病中的治疗潜力。(C) 2019 Elsevier Inc.版权所有。
Background: Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyper proliferation. Ginsenoside compound K (CK), a bioactive metabolite of ginseng, modulates various skin disorders with an impact on keratinocyte biology. However, the effect of Ginsenoside CK in psoriasis has not been explored.Objective: Our aim was to investigate whether ginsenoside CK could affect the homeostasis of keratinocytes and their expression of psoriasis-associated antimicrobial protein regenerating islet-derived protein 3-alpha (REG3A) and its murine ortholog RegIII gamma. We further explored the therapeutic potential of ginsenoside CK in imiquimod (IMQ)-induced psoriasis-like dermatitis.Methods: The effects of ginsenoside CK in cell growth and apoptosis of human keratinocytes were measured by MTT assay and flow cytometry, respectively. Bax levels were evaluated by Western blot in HaCaT cells following ginsenoside CK stimulation. REG3A levels were assessed by RT-PCR and Western blot in human keratinocytes following interleukin (IL)-36 gamma and ginsenoside CK co-simulation. Utilizing IMQ-induced psoriasis mouse model, the therapeutic effects of 0.1% and 1% ginsenoside CK cream were assessed by skin thicknesses and histological examinations, and RegIII gamma level in the lesional skin was detected by Western blot and immunofluorescence.Results: Ginsenoside CK prohibited human keratinocyte proliferation but did not affect their apoptosis. Moreover, it inhibited 1L-36 gamma-induced REG3A expression in HaCaT cells. Ginsenoside CK alleviated imiquimod-induced psoriasis-like hyperkeratosis and reduced RegIII gamma expression in the keratinocytes from lesional skin.Conclusion: Ginsenoside CK ameliorated IMQ-induced psoriasis-like dermatitis possibly through inhibiting REG3A/RegIII gamma expression in keratinocytes, which highlighted a therapeutic potential of ginsenoside CK in psoriasis. (C) 2019 Elsevier Inc. All rights reserved.